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CONTINUING PROFESSIONAL DEVELOPMENT

Page 58
The assessment and
management of venous
thromboembolism

Page 66
Venous thromboembolism
multiple choice
questionnaire

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The assessment and management

of venous thromboembolism
NS334 Welch E (2006) The assessment and management of venous thromboembolism.
Nursing Standard. 20, 28, 58-64. Date of acceptance: September 9 2005.

Identify which patients will benefit from
prophylactic measures.

Summary
This article examines venous thromboembolism (VTE) and offers
guidance on its prevention. VTE is a potentially fatal condition,
which can be prevented using both pharmacological and mechanical
methods. Nursing staff should be aware of the risk factors that
predispose patients to venous thromboembolism and ensure that
high-risk patients receive the prophylaxis they require.

Author
Ellen Welch is a senior house officer, Nelson Hospital, Hamilton,
New Zealand. Email: welchellen@yahoo.co.uk

Keywords

Discuss the treatment options and nursing

interventions available to patients with VTE.

Time out 1
Before reading on, summarise what you
know already about VTE. How does it present
in practice, and which patients are most at risk?

Introduction

Recognise the signs and symptoms of deep vein

thrombosis (DVT) and pulmonary
embolism (PE).

In March 2005, the House of Commons Health

Committee published a critical report on the
prevention of VTE. The report states that more
than 25,000 patients in England die each year
from VTE, which is more than the combined total
of deaths from breast cancer, acquired immune
deficiency syndrome and road traffic injuries
(House of Commons Health Committee 2005).
Many of these deaths are preventable. By
recognising high-risk patients, and starting them
on what is proven to be a safe and cost-effective
prophylactic treatment, lives can be saved. At
present, no national guidelines exist to ensure that
health professionals consider the risk of VTE, but
the National Institute for Health and Clinical
Excellence (NICE) has been commissioned to
address this problem and a report is expected to
be published in May 2007 (House of Commons
Health Committee 2005). In the meantime, it is
important that nurses can recognise patients at
risk from VTE and implement prophylaxis.

Summarise the pathophysiology associated

with the formation of VTE.

Pathophysiology

List the risk factors that predispose patients

to VTE.

Venous thrombosis is a condition in which a

blood clot (thrombus) forms in a vein. This

Deep vein thrombosis; Thrombosis; Vascular disorders

These keywords are based on the subject headings from the British
Nursing Index. This article has been subject to double-blind review.
For related articles and author guidelines visit our online archive at
www.nursing-standard.co.uk and search using the keywords.

Aims and intended learning outcomes

This article aims to provide an update and
overview of venous thromboembolism (VTE) and
its clinical presentation. It discusses management
strategies and how to recognise at-risk patients to
initiate prophylactic measures in hospital. After
reading this article you should be able to:

Outline the clinical manifestation of VTE.

58 march 22 :: vol 20 no 28 :: 2006

NURSING STANDARD

manifests clinically as DVT, commonly in the

deep veins of the legs, thighs and pelvis; and PE if
the clot breaks off from the site in which it was
created and lodges in the lung vessels (House of
Commons Health Committee 2005). DVT and
PE are collectively known as VTE (Box 1).
Thrombus formation is a result of an
imbalance between the anticoagulant and
procoagulant systems in the blood (Enders et al
2002). Three pathological processes, known
collectively as Virchows triad, have been shown
to promote this imbalance (United Kingdom (UK)
Venous Thromboembolism Registry (VERITY)
2004). Patients with venous trauma (problems
with the vessel wall), venous stasis (problems
with blood flow) or hypercoagulability (problems
with the bloods clotting components) are
predisposed to VTE formation (Box 2).
Clotting Clot formation is a complex process in
which fibrinogen, a soluble protein in blood, is
converted to a fibrin clot by the action of
thrombin. This process is important in reducing
blood loss when vessels are damaged or
ruptured (Kumar and Clark 2002). Injury to
vessel walls exposes collagen and releases tissue
factor, a protein expressed by cell surfaces. This
leads to a complex cascade of reactions in
which various coagulation factors activate one
another (Enders et al 2002). Although this
process is important in the repair of damaged
vessels, the clotting cascade can be initiated in
high-risk patients, resulting in thrombus
formation and causing symptoms of VTE
(Kumar and Clark 2002).

Time out 2
What clinical signs and symptoms
would lead you to suspect a DVT or PE?

Deep vein thrombosis

syndrome, which increases the risk of recurrent

VTE (Geerts et al 2004). DVT can resolve
completely without causing patients any ill
effects, but its prevention and treatment are
important, since it can lead to a fatal PE.

Time out 3
Reflect on the investigations you
have seen carried out on a patient
with suspected DVT or PE and make a list
of these.
Investigations Clinical diagnosis of DVT is often
unreliable, so combinations of diagnostic
investigations are usually performed. The gold
standard for establishing a diagnosis of DVT is
contrast venography, but since this procedure is
invasive and expensive it is rarely used (Tovey and
BOX 1
Glossary
Deep vein thrombosis (DVT): venous thrombosis that occurs in the deep
veins of the legs, thighs or pelvis.
Post-thrombotic (post-phlebitic) syndrome: chronic pain and swelling
and occasional ulceration of the skin, occurring as a consequence of
previous venous thrombosis.
Pulmonary embolism (PE): a blood clot that breaks off from the deep
veins and travels round the circulation to block the pulmonary arteries.
Most deaths arising from DVT are caused by PE. A massive PE is one so
severe as to cause circulatory collapse.
Venous thromboembolism (VTE): the blocking of a blood vessel by a clot
dislodged from its site of origin. It includes both DVT and PE.
Venous thrombus: a condition in which a blood clot (thrombus) forms in
a vein.
(British Thoracic Society (BTS) 2003, House of Commons Health Committee 2005)

BOX 2
Virchows triad

DVT usually begins when small deposits of fibrin

collect in the deep veins of the thigh or calf as a
result of slow blood flow and local activation of
the clotting cascade. DVT can be asymptomatic,
but the classic symptoms of calf pain, swelling,
increased skin temperature, superficial venous
dilation and (occasionally) pitting oedema
usually occur when a thrombus becomes large
enough to cause blood outflow problems
(Gorman et al 2000). Complete occlusion of a
vein is rare, but can lead to a cyanotic
discoloration of the limb and severe oedema,
which can develop into venous gangrene (Kumar
and Clark 2002).
Venous thrombosis usually occurs around the
cusp of a venous valve (Sevitt 1974). This can
cause irreversible valve damage, leading to
chronic venous insufficiency or post-thrombotic
NURSING STANDARD

1. Venous trauma
Trauma or damage to vascular endothelium as a result of infection can lead
to the release of tissue factor which initiates the extrinsic clotting cascade
leading to clot formation.
2. Venous stasis
Vessel compression by enlarged lymph nodes, bulky tumours, or previous
thromboses can lead to venous stasis, as can immobility or confinement to
bed one of the main reasons that hospital inpatients are at increased risk
of venous thromboembolism (VTE).
3. Hypercoagulability
Genetic conditions such as thrombophilia, which affects one in 20 of the
United Kingdom population and causes the blood to clot more easily than
it should, increasing the chances of thrombus formation. Cancers,
particularly adenocarcinomas and metastatic cancers, and oestrogens,
found in oral contraceptives and hormone replacement therapy, can also
activate the clotting system, increasing the risk of VTE.
(Enders et al 2002, Turpie et al 2002a, House of Commons Health Committee 2005)

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learning zone vascular nursing

BOX 4
Unfractionated heparin vs low molecular
weight heparin

Wyatt 2003). In practice, ultrasonography

combined with a d-dimer blood test (Box 3) is
usually carried out. Ultrasound is not 100 per
cent reliable, and those patients who are clinically
suspected of having a DVT but have a negative
ultrasound result should ideally have the test
repeated a week later (Turpie et al 2002a).
Treatment DVT and PE are treated similarly. Low
molecular weight heparin (LMWH) is given to
patients with suspected VTE and, once diagnosis
is confirmed, patients are started on oral
anticoagulation with warfarin. Box 4 summarises
why LMWH has replaced unfractionated heparin
as the treatment of choice.
Warfarin is the most widely used oral
anticoagulant and works by antagonising the
effects of vitamin K. It is teratogenic (may cause
serious embryonic or fetal malformation) and
should not be given in the first trimester of
pregnancy. It is known to interact with a number
of drugs including alcohol (British National
Formulary (BNF) 2005). The anticoagulant
effects of warfarin take at least 48 to 72 hours to
develop fully, so it is important that heparin is
given concomitantly (BNF 2005). The usual
starting dose of warfarin is 10mg daily for two
days and the subsequent maintenance dose varies
between patients and depends on the
prothrombin time, which is reported universally
as the international normalised ratio (INR). A
target INR range of 2-3 is standard for treatment
of VTE, and patients should be monitored for
signs of bleeding (Turpie et al 2002b). The INR
should be measured daily in the early days of
treatment, then at longer intervals depending on
the response (BNF 2005).
BOX 3
D-dimer blood test
D-dimers are protein derivatives of fibrin found in
plasma and produced when fibrin is degraded by
plasmin (also known as fibrin degradation products).
Plasma concentrations of d-dimers are therefore raised
in patients with venous thromboembolism (VTE). A
positive diagnosis of VTE cannot be made using a
d-dimer blood test alone, since levels can also be raised
during infection, malignancy, pregnancy and after an
operation. D-dimers have a high negative predictive
value, so if a patient with suspected VTE has a normal
d-dimer blood test, the diagnosis can be ruled out.
D-dimer testing is not indicated in patients with a high
clinical probability of pulmonary embolism, since the
test is almost certainly going to be positive and adds
little to the clinical picture.
(BTS 2003, Tovey and Wyatt 2003)

60 march 22 :: vol 20 no 28 :: 2006

In the past, unfractionated heparin was the initial

treatment for venous thromboembolism (VTE) and
was administered by continuous infusion. This method
required daily monitoring of activated partial thromboplastin time (APTT) with adjustment of dose according to the response of each patient. Heparin use for
more than six days is also associated with an
increased risk of thrombocytopenia (a reduction in the
number of platelets in the blood).
Low molecular weight heparin (LMWH) has a more
predicable relation between dose and response based on
a patients body weight, so does not require such close
monitoring. It is associated with a lower risk of thrombocytopenia, no excess bleeding and can be administered by patients at home. For these reasons, LMWH
has largely replaced the use of unfractionated heparin.
(Turpie et al 2002b)

Heparin treatment should continue alongside

warfarin therapy for at least five days or until the
INR is greater than 2 (Turpie et al 2002b).
Anticoagulation with warfarin should continue
for at least three months, although longer
treatment regimens are recommended in certain
patients (Box 5).

Pulmonary embolism
PE occurs when a thrombus or other foreign
substance lodges in a pulmonary blood vessel and
obstructs circulation to the lung tissue. Classic
symptoms include breathlessness and tachypnoea,
pleuritic chest pain and occasionally haemoptysis.
In the instance of a massive PE, leading to cardiac
arrest, patients may collapse, become hypotensive
and hypoxic and may show signs of engorged neck
veins and a right ventricular gallop (a loud,
additional heart rhythm) (BTS 2003).
Investigations Patients with suspected PE should
have initial routine investigations including chest
X-ray, electrocardiogram (ECG) and arterial blood
gases to exclude other causes. A negative d-dimer
blood test can reliably exclude diagnosis in patients
considered low probability for PE, and further
imaging is not required in such patients. Patients
with a high clinical probability of PE (that is,
multiple risk factors and ECG changes suggestive of
PE), and those with low to intermediate probability
but with a positive d-dimer blood test should have
further investigations. Isotope lung scanning
(commonly known as a ventilation-perfusion or
V/Q scan) is usually the initial investigation
implemented, but has been found to generate a
significant number of false positive results. It is also
unreliable in patients with chronic cardiac or
respiratory disease. In these cases, patients go on to
have a computed tomographic pulmonary
NURSING STANDARD

angiography (CTPA), which is quicker to perform,

rarely needs to be followed by other imaging and
may provide the correct diagnosis if PE is excluded.
Ideally this should be the first-line investigation
used, but current resources make this impractical
(BTS 2003). Since 70 per cent of patients with
proven PE have proximal DVT, ultrasound
scanning of the legs has also been suggested as the
initial imaging test to confirm VTE (BTS 2003).
A clinically massive PE can be reliably
diagnosed with CTPA and echocardiography.
Such imaging should be performed within one
hour of presentation and within 24 hours in
non-massive PE (BTS 2003).
Treatment Supportive therapy with oxygen and
analgesia should be initiated as indicated. In
patients with massive PE where cardiac arrest is
imminent, thrombolysis with a bolus of 50mg
alteplase is recommended, although this should
not be used as a first-line treatment in
non-massive PE (BTS 2003). Invasive
approaches, that is, inferior vena caval filter
insertion or thrombus fragmentation, should be
considered where the facilities and expertise are
readily available (BTS 2003).
Anticoagulation therapy for patients with PE is
the same as described above for treatment of DVT.
Complications The majority of PEs are reabsorbed
spontaneously and cause no ill effects once
treated. The altered blood flow and impaired gas
exchange caused by a massive PE, however, result
in decreased pulmonary compliance or even
pulmonary infarction, leading to haemodynamic
compromise which can be fatal. Patients who
survive may have increased pulmonary vascular
resistance which can lead to pulmonary
hypertension and heart failure (Enders et al 2002).

Risk factors
Surgery and acute myocardial infarction (MI) are
well-recognised major risk factors for VTE and, as a
consequence, these groups of patients are routinely
provided with prophylaxis (Anderson and Spencer
2003). General medical patients are also at risk.
Post-mortem studies estimate that 10 per cent of
hospital deaths can be attributed to PE; 70 per cent
of these occurring in medical patients and three
quarters of which were unrecognised before
post-mortem (Gerotziafas and Samama 2004).
Factors that promote venous stasis,
hypercoagulability or vascular damage
contribute to the risk of VTE. Table 1 shows
factors that increase this risk, as agreed by the
American College of Chest Physicians (ACCP)
and the Thromboembolic Risk Factors
Consensus Group (THRIFT 1992).
The more risk factors a person has, the greater
his or her risk of developing VTE (Anderson et al
1992). Prophylaxis in hospitalised patients is
NURSING STANDARD

BOX 5
Duration of anticoagulation therapy for
venous thromboembolism (VTE)
Three to six months: patients with first event VTE
with reversible or time-limited risk factors.*
More than six months: patients with idiopathic VTE
(first event).
One year to life:

Patients with first event VTE with cancer (until
resolved), anticardiolipin antibody, antithrombin
deficiency.

Patients with recurrent events idiopathic or with
thrombophilia.
* Reversible or time-limited risk factors include
surgery, trauma, immobilisation and oestrogen use.
(Hirsh 1995, Turpie et al 2002b)

extremely important since they often have

multiple risk factors (THRIFT 1992, Verstraete
1997, Geerts et al 2004).
Long-haul travel The risk of VTE in people
travelling on long-haul flights has been widely
publicised, but the actual risk of death from
flight-related VTE is estimated at one per two
million passengers arriving from a flight (Kelman
et al 2003). It is thought that the immobility, low
atmospheric pressure and dehydration associated
with prolonged air travel may increase the risk of
developing VTE (Kelman et al 2003), and the
greater the distance travelled, the more at risk
patients become (Lapostolle et al 2001). Despite
this, long-haul travel as a risk factor for VTE in its
own right still remains to be proven conclusively
(Hirsh and ODonnell 2001).
The ACCP recommends that travellers on
flights lasting six hours or more should ensure
adequate hydration, avoid constrictive clothing
and stretch their calf muscles frequently. Those at
risk of VTE may benefit from properly fitted
below-knee compression stockings or a dose of
LMWH, but aspirin is not recommended because
there is not enough evidence supporting its use in
VTE prevention (Geerts et al 2004).

Evidence for prevention

The NICE guidelines on VTE prophylaxis, due to
be published in 2007, will only outline
interventions for thromboprophylaxis in surgical
patients (House of Commons Health Committee
2005). There is evidence to suggest that medical
inpatients are at as much risk as those undergoing
surgery, and that guidelines should be in place
throughout the UK to ensure medical patients are
protected against VTE (Geerts et al 2004).
The UK national venous thromboembolism
registry recorded 2,720 cases of VTE between
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learning zone vascular nursing

December 2001 and November 2003. Twelve per
cent (n=323) of these cases had recently had a
hospital stay as a medical inpatient compared to
the 10 per cent (n=265) who had undergone
recent surgery, suggesting that acute medical
illness is an independent risk factor for VTE
(UK VERITY 2004). In the United States, it has
been recommended that all medical inpatients
with one or more risk factor for VTE should
receive thromboprophylaxis (Geerts et al 2004),
and computer-alert programmes are being
instituted to remind practitioners of this (Poller et
al 1998, Kucher et al 2005).
Patients with contraindication to heparin
prophylaxis, or those at high risk of bleeding
are advised to use mechanical prophylaxis
such as graduated compression stockings (Geerts
et al 2004).

Pharmacological prophylaxis
The ACCP recommends pharmacological
prophylaxis with either unfractionated heparin
or LMWH in all acutely ill medical patients who
have one or more risk factors for VTE (Geerts et
al 2004). Surgical patients should also continue to
be given prophylaxis on admission since LMWH
prophylaxis reduces the risk of VTE in general

surgery patients by more than 70 per cent

compared with placebo (Mismetti et al 2001). A
meta-analysis carried out by Mismetti et al (2000)
showed that unfractionated heparin and LMWH
are equally effective at reducing the incidence of
VTE, but LMWH is safer with a 52 per cent lower
risk of bleeding. The MEDENOX (Samama et al
1999) and PREVENT (Leizorovicz et al 2004)
randomised controlled trials investigated the
efficacy of LMWH. Both found the incidence of
DVT to be reduced.

Time out 4
Consider the following scenarios.
Should prophylactic low molecular
weight heparin (LMWH) be given to the
following patients:

A fully mobile 31-year-old female smoker
admitted to the acute medical admissions
unit with a severe chest infection?

A 40-year-old male with a body mass index of
35 (obese), who is usually fit and well and has
presented to hospital with gastroenteritis?
According to the ACCP guidelines, both
patients have risk factors for VTE, and should
be given LMWH. Do you agree and if so, why?
LMWHs have a longer duration of action than
unfractionated heparins, allowing for once daily
subcutaneous dosage and the standard
prophylactic regimen does not require

TABLE 1
Risk factors for venous thromboembolism
Background factors

Disease or surgical procedure

Activated protein C resistance

Behets disease

Age more than 40 years

Central venous catheterisation

High-dose oestrogens

Heart failure

Homocystinaemia (an amino acid disorder that causes

an excess of homocystine in the blood)

Inflammatory bowel disease

Immobility (bed rest more than four days)

Phospholipid antibody or lupus anticoagulant
Pregnancy and postpartum
Previous deep vein thrombosis or pulmonary embolism
Puerperium
Severe obesity
Smoking
Thrombophilia: deficiency of antithrombin III,
protein C, protein S
Varicose veins

Malignancy, especially pelvic or abdominal

Nephrotic syndrome
Paralysis of lower limb(s)
Paraproteinaemia (the presence of abnormal proteins in the blood)
Paroxysmal nocturnal haemoglobinuria (a disorder characterised
by blood in the urine because of an abnormality of the red cell
membrane)
Polycythaemia (increase in haemoglobin content of blood)
Recent myocardial infarction
Respiratory failure
Severe infection
Trauma or surgery, especially of pelvis, hip, and lower limb

(THRIFT 1992, Verstraete 1997, Geerts et al 2004)

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NURSING STANDARD

monitoring (BNF 2005). Several types of LMWH

are licensed for use in VTE prevention, but
protocols remain to be established for exact
prophylactic dose regimens. Table 2 outlines the
typical recommended doses available.
LMWH is given via subcutaneous injection, a
procedure with which nursing staff should be
familiar. Box 6 provides practical information on
administering a subcutaneous injection.

Time out 5
For which patients should
antiembolism stockings be avoided? How
would you assess and care for a patient who
requires antiembolism stockings?

Nursing interventions
All patients should be assessed for risk of VTE on
admission to hospital, remembering that medical
patients can be at as much risk as surgical patients.
Methods of prophylaxis are aimed at targeting the
three predisposing factors (venous stasis, venous
trauma and hypercoagulability), using
pharmacological and mechanical interventions.
Antiembolism stockings have been found to
prevent venous dilation (Coleridge Smith et al
1991) and improve blood flow by stimulating
fibrinolytic activity within blood vessels (Arcelus et
al 1995). The use of compression stockings has also
been found to significantly reduce post-thrombotic
syndrome (Brandjes et al 1997). Nurses should
assess all patients for any contraindications to
antiembolism stockings, avoiding their use in
patients with arterial impairment or leg ulcers.
Many stockings contain latex, so alternate
brands should be used for patients with a latex
allergy. All patients should be measured to
ensure that they receive the correct size of
stocking, and should be given information on
how to wear and care for their antiembolism
stockings (Box 7).
FIGURE 1
Anatomical sites for subcutaneous injection

BOX 6
Practical information on subcutaneous
injection

After explaining the procedure to the patient,
checking the correct drug, dose, date and time of
administration, start by choosing an appropriate
injection site and clean the area with an alcohol
swab. Sites used for subcutaneous injection are
shown in Figure 1.

Using the non-dominant hand, gently pinch the
skin over the site. Insert the needle into the skin at
a 45 angle, releasing the skin once the needle is
in position to reduce discomfort and ensure the
drug is delivered into the subcutaneous tissue.

Withdraw the piston of the syringe. If any blood is
drawn up, then withdraw the needle and start the
procedure again at a different site. This ensures
the drug is not injected directly into a blood vessel.

If no blood is withdrawn, inject slowly then
withdraw the needle quickly. Apply pressure to any
bleeding, document administration and ensure all
sharps are disposed of correctly.
(Mallett and Dougherty 2000)

BOX 7
Fitting antiembolism stockings
Nurses should refer to manufacturers literature when
measuring and fitting patients for antiembolism
stockings. The general procedure shown on the
following website and taken from Kendalls TED
antiembolism stocking product packing, should apply
to most brands:
www.newlook.com.sg/info.asp?key=TED%20ApplyThB
(Last accessed: March 7 2006.)
Patients should be told the following information:

Stockings should be smooth when fitted.

The toe hole should lie underneath the toes.

The heel patch should be in the correct position.

The thigh gusset should be on the inner thigh.

Rolling down the stockings may have a tourniquet
effect.
(Bonner 2004)

TABLE 2
Typical recommended doses of low molecular weight
heparin (LMWH)
Subcutaneous injection once daily
LMWH preparation

Low to moderate risk

High risk

Enoxaparin

2,000 iu

4,000 iu

Tinzaparin

3,500 iu

4,500 iu

Dalteparin

5,000 iu

5,000 iu

(Geerts et al 2004, BNF 2005)

NURSING STANDARD

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learning zone vascular nursing

Skin integrity should be regularly checked, and
patients should be advised to report any feelings
of tingling or numbness. Early mobilisation
should be encouraged and nurses can teach
patients leg and breathing exercises to stimulate
the calf muscle pump and aid venous return
(Bonner 2004).

Conclusion
VTE is a potentially fatal condition, which can
be prevented using both pharmacological and

mechanical methods. LMWH for VTE

prophylaxis is underused in the UK at present,
despite evidence that it is effective. It is
important that nurses are aware of the risk
factors of patients in their care, and ensure that
high-risk patients are receiving the prophylaxis
they require NS

Time out 6
Now that you have completed this
article, you might like to consider writing
a practice profile. Guidelines are on page 68.

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